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Overall, these data demonstrate the existence of an enhanced neuroinflammation status in old brain, as demonstrated by the higher amount of proinflammatory and stress-associated mediators in older mice compared with the younger ones. Moreover, these factors are mainly expressed in the hippocampal region compared with the cortex. The same pattern of genes was analysed to compare sham and SNI mice coupled on the basis of brain area and injury duration (Fig. 6). As a result, we observed the significant upregulation of 26 genes in the hippocampus of the 1-month SNI mice compared with the 1-month sham animals (Fig. 6A and B). Among these genes, there are the apoptosis-related factors Bax and Bcl-2 (3.4 and 4.3-fold), the endothelial marker CD34 (3.4-fold), the pan-macrophage marker CD68 (3.4-fold), the ADP-ribosyl cyclase CD38 (3.6-fold), which acts as a regulator of neuroinflammatory processes in astrocyte-induced neuroprotection, CCR2 (4.3-fold), and macrophage colony-stimulating factor-1 (4.4-fold). A substantial upregulation of the proinflammatory cytokines IL18, IL1B, and IL7 (2.6-fold, 3.5-fold, and 9.6-fold, respectively) was also recorded, together with the inflammatory mediators PTGS2, NFkB1 and 2, STAT6, and IKBKB by 2.7-fold, 5.0-fold, 2.5-fold, 3.3-fold, and 6.9-fold, respectively. The activation of the classical pathway of the complement system was also revealed by 5.3-fold upregulation of C3 gene. A possible rebound effect of these multiple proinflammatory stimuli could be the reason for the huge increase of SOCS2 expression (11.1-fold). The immunosuppressive cytokine TGF-b1, which acts as a pivotal controller of cell growth and differentiation and of tissue repair after injury, was upregulated by 3.2-fold, but a simultaneous induction of its negative regulator SMAD7 (3.7-fold) was observed too. The expression of angiogenic factors EDN1 and VEGFA, as well as the adhesion molecule VCAM1, was also found strongly induced (3.6-, 6.5-, and 3.4-fold, respectively). Worthy of note is the huge induction of transferrin receptor (TFRC, 5-fold). The PANTHER software revealed the representation of the most affected pathways in the hippocampus of the 1-month SNI mice compared with the 1-month sham animals (Fig. S3C, available at http://links.lww.com/PAIN/B547), showing 8 genes involved in inflammation mediated by chemokine and cytokine signaling pathways, 5 genes in apoptotic pathway, 4 in CCKR map, other 4 in Toll receptor signaling pathway, and other genes variously involved in B-cell activation, T-cell activation, TGF-b, Wnt, PDGF, and endothelin signaling pathways.